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Adult-onset deficiency in growth hormone and insulin-like growth factor-I alters oligodendrocyte turnover in the corpus callosum

✍ Scribed by Kun Hua; M. Elizabeth Forbes; Robin J. Lichtenwalner; William E. Sonntag; David R. Riddle

Publisher
John Wiley and Sons
Year
2009
Tongue
English
Weight
283 KB
Volume
57
Category
Article
ISSN
0894-1491

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✦ Synopsis

Abstract

Growth hormone (GH) and insulin‐like growth factor‐I (IGF‐I) provide trophic support during development and also appear to influence cell structure, function and replacement in the adult brain. Recent studies demonstrated effects of the GH/IGF‐I axis on adult neurogenesis, but it is unclear whether the GH/IGF‐I axis influences glial turnover in the normal adult brain. In the current study, we used a selective model of adult‐onset GH and IGF‐I deficiency to evaluate the role of GH and IGF‐I in regulating glial proliferation and survival in the adult corpus callosum. GH/IGF‐I‐deficient dwarf rats of the Lewis strain were made GH/IGF‐I replete via twice daily injections of GH starting at postnatal day 28 (P28), approximately the age at which GH pulse amplitude increases in developing rodents. GH/IGF‐I deficiency was initiated in adulthood by removing animals from GH treatment. Quantitative analyses revealed that adult‐onset GH/IGF‐I deficiency decreased cell proliferation in the white matter and decreased the survival of newborn oligodendrocytes. These findings are consistent with the hypothesis that aging‐related changes in the GH/IGF‐I axis produce deficits in ongoing turnover of oligodendrocytes, which may contribute to aging‐related cognitive changes and deficits in remyelination after injury. © 2008 Wiley‐Liss, Inc.

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